Centre for Human and Applied Physiology, School of Medicine, University of Wollongong, Wollongong, NSW, 2522, Australia.
Centre for Human and Applied Physiology, School of Medicine, University of Wollongong, Wollongong, NSW, 2522, Australia.
J Therm Biol. 2019 Jul;83:37-46. doi: 10.1016/j.jtherbio.2019.05.001. Epub 2019 May 3.
To better understand the relationships between changes in body temperature and displacements of the thermoeffector thresholds (critical temperatures), the passive cooling (and heating) of pre-heated (and pre-cooled) individuals was investigated. Such experiments are necessary to understand the inter-dependence of those thresholds, and may possibly yield human evidence for the existence of separate central controllers. Eight males participated in four trials; two when normothermic, one following pre-experimental heating and the fourth following pre-cooling. Subjects were exposed to passive, whole-body cooling and heating when normothermic (the control trials), and again following pre-heating and pre-cooling (respectively). Cutaneous vasomotor, thermogenic, as well as precursor and discharged sudomotor thresholds from different body segments were compared across those dynamic thermal states. Following pre-heating, the critical mean body temperatures for vasoconstriction (0.37 °C ± 0.10) and thermogenesis (0.67 °C ± 0.20) were significantly elevated during passive cooling, relative to the corresponding control trial (both P < 0.05). When passive heating followed pre-cooling, the thresholds for vasodilatation were reduced (0.37 °C ± 0.07; P < 0.05). Conversely, but with the exception of forehead precursor sweating, the sudomotor thresholds were elevated (averaging 0.16 °C ± 0.02; P < 0.05). Most thermoeffectors revealed unique and adjustable activation thresholds, with the threshold displacements for thermogenesis and vasomotion appearing to be linked to the change in mean body temperature. Following pre-cooling, the critical temperatures for vasodilatation and sudomotor activation varied independently, with the exception of forehead precursor sweating. Collectively, those observations are consistent with the presence of independent central controllers for thermally dependent vasomotor and sudomotor responses, and perhaps also for shivering thermogenesis.
为了更好地理解体温变化与热敏效应器阈值（临界温度）位移之间的关系，研究了对预热（和预冷）个体进行被动冷却（和加热）的情况。这些实验对于理解这些阈值之间的相互依存关系是必要的，并且可能为独立的中央控制器的存在提供人体证据。8 名男性参加了 4 项试验；2 项在体温正常时，1 项在实验前加热后，第 4 项在预冷却后。当体温正常时（对照试验），以及在预热和预冷后（分别），受试者接受被动的全身冷却和加热。在这些动态热状态下，比较了来自不同身体部位的皮肤血管舒缩、产热以及前体和排出性出汗阈值。预热后，在被动冷却期间，与相应的对照试验相比，血管收缩（0.37°C±0.10）和产热（0.67°C±0.20）的临界平均体温显著升高（均 P<0.05）。当被动加热紧随预冷却之后，血管扩张阈值降低（0.37°C±0.07；P<0.05）。相反，除了额前前体出汗外，出汗阈值升高（平均 0.16°C±0.02；P<0.05）。大多数热敏效应器显示出独特且可调节的激活阈值，产热和血管运动的阈值位移似乎与平均体温的变化有关。预冷却后，血管扩张和出汗激活的临界温度独立变化，除了额前前体出汗。总的来说，这些观察结果与存在独立的中央控制器来控制热依赖性血管舒缩和出汗反应，以及可能还有寒战产热是一致的。
